Transcript Toxoplasmosis

Toxoplasmosis is a zoonotic disease caused by
infection with the protozoan Toxoplasma gondii
 Toxoplasmosis may cause flu-like symptoms in
some people, but most people affected never develop
signs and symptoms.
 For infants born to infected mothers and for people
with weakened immune systems, toxoplasmosis can
cause extremely serious complications.

• An obligate intracellular parasitic protozoan.
• T. gondii is capable o f infecting virtually all warm-blooded animals(lack
of host specificity).
• Cats are the definitive hosts in which the parasite can undergo sexual
reproduction.
• During infection two forms of parasite may form:
– Tackyzoit: Rapidly growing form (acute infection).
– Bradyzoit: Slowly growing form in cysts ( chronic infection).
• Tissue cysts formed in any organ especially brain, eyes and strained
muscles.
• Eating undercooked, contaminated meat .
• Eating food that was contaminated by knives,
utensils, cutting boards and other foods that have
had contact with raw, contaminated meat (cross
contamination).
• Drinking water contaminated with Toxoplasma
gondii.
• Mother-to-child (congenital) transmission.
• Accidentally swallowing the parasite through
contact with cat feces that contain Toxoplasma.
• Receiving an infected organ transplant or
infected blood via transfusion, though this is
rare.
• Toxoplasmosis is usually nothing to worry about because the
immune system is normally strong enough to fight the infection and
stop it from causing serious illness. After getting the infection, most
people are immune to it for the rest of their life.
• However, it can lead to serious problems in:
– women who become infected while they're pregnant .
– people with weak immune systems.
• Approximately 10-20% of pregnant women infected with T
gondii become symptomatic, The most common signs of
infection are lymphadenopathy and fever.
• When a mother is infected with T gondii during gestation,
the parasite may be disseminated hematogenously to the
placenta. When this occurs, infection may be transmitted to
the fetus transplacentally.
If infection was shortly before conception
(within a few weeks before) :
– carries a one percent risk or below of transmission to the
baby, but there is a risk of miscarriage if the baby does become
infected.
If infection was in the first trimester (week one to 12)
– carries about 10-15 percent risk of transmission to the baby. A baby
infected at this stage has a risk of being miscarried or stillbirth.
If infection was in the second trimester (week 13 to
28):
–about 25 percent risk of transmission. A baby
infected at this stage is less likely to be miscarried,
but is still at risk of developing severe symptoms as:
• Hydrocephaly (water on the brain)
• Calcifications of the brain
• Retinochoroiditis (inflammation of the
retina)blindness
• Microcephaly.
• Neurological disorders.
If infection was in the third trimester (week 29 to 40)
–Risk of transmitting the infection rises again if
toxoplasmosis is caught at this stage of pregnancy, and
may be as high as 70–80 percent.
–Most babies infected will be apparently healthy at birth,
but a large proportion will develop symptoms later in
life, usually eye damage and Neurological problems .
Retinochoroiditis (ocular toxoplasmosis)
• Retinochoroiditis usually results from
reactivation of congenital infection, or a part
of acute infection.
• When the organism reaches the eye through
the bloodstream, depending on the host's
immune status, a clinical or subclinical focus of
infection begins in the retina.
• As the host's immune system responds, the cyst forms which is
resistant to the host's immune system, and a chronic, latent
infection ensues.
• The cyst remains in the normal-appearing retina. Whenever the
host's immune function declines for any reason, the cyst wall
rupture, releasing organisms into the retina, and the
inflammatory process starts. If an active clinical lesion is
present, healing occurs as a retinochoroidal scar.
serologic tests.
 Amplification of specific nucleic acid sequences (i.e.,
polymerase chain reaction [PCR]).
Histologic demonstration of the parasite and/or its antigens
(i.e., immunoperoxidase stain).
Isolation of the organism.
Other rarely used methods include:

– demonstration of antigen in serum and body fluids.
– A toxoplasmin skin test.
– antigen-specific lymphocyte transformation.
• Serologic testing:
• Different serological tests often measure
different antibodies that possess unique
patterns of rise and fall with time after
infection.
• A combination of serological tests is
frequently required to establish whether an
individual has been more likely infected in
the distant past or has been recently
infected.
• IgG antibodies:
– IgG antibodies usually appear within 1–2 weeks of
acquisition of the infection, peak within 1–2 months,
decline at various rates, and usually persist for life.
– The most commonly used tests for the measurement
of IgG antibody are the Sabin-Feldman Dye Test (DT),
ELISA, IFA, and the modified direct agglutination test.
• IgM antibodies:
– IgM antibody titres rise from 5 days to weeks following
acute infection, reaching a maximum within 21 days
and decline more rapidly than IgG.
– The most commonly used tests for the measurement
of IgM antibody are ELISA kits, the IFA test, and the
immunosorbent agglutination assay (ISAGA).
Note: Ecteric phase is the period when switching b/w IgG and
IgM production , results in low levels of both.
• IgA Antibodies:
– IgA antibodies may be detected in sera of acutely infected
adults and congenitally infected infants using ELISA or
ISAGA methods.
– It appears in sera when the parasite attacks the eye
(toxoplasmic chorioretinitis).
– In a number of newborns with congenital toxoplasmosis
and negative IgM antibodies, the serological diagnosis
has been established by the presence of IgA and IgG
antibodies.
• IgE Antibodies:
– IgE antibodies are detectable by ELISA in sera of acutely infected
adults, congenitally infected infants.
– The duration of IgE seropositivity is less than with IgM or IgA
antibodies and hence appears useful as an adjunctive method for
identifying recently acquired infections.
• Histologic diagnosis:
– Diagnosis also can be made by direct observation of the parasite in
stained tissue sections from biopsy.
– Immunoflorscence stain and sabin field man stain can be used.
– These techniques are used less frequently because of the difficulty of
obtaining these specimens.
• Isolation:
– Parasites can also be isolated from blood or other body fluids by
animal inoculation or cell cultures, but this process can be
difficult and requires considerable time.
• PCR:
– Molecular techniques that can detect the parasite's
DNA in the amniotic fluid can be useful in cases of
possible mother-to-child (congenital) transmission.
– Amniocentesis:
• to identify T. gondii in the amniotic fluid by PCR (the most
sensitive and specific), done if serologic testing cannot
confirm or exclude acute infection, and if there are abnormal
ultrasound findings suggestive of toxoplasmosis infection.
– Fetal blood sampling (cordocentesis):
• was previously the gold standard for diagnosing fetal
infection but no longer, because of the associated higher
fetal risk
• Ocular disease is diagnosed based on
the appearance of the lesions in the
eye, symptoms, course of disease,
and often serologic testing and
measuring the level of IgA.
• There are 2 goals of drug therapy for toxoplasmosis, depending
on whether or not fetal infection has occurred.
– If maternal infection has occurred but the fetus is not infected,
spiramycin is used for fetal prophylaxis (to prevent spread of
organisms across the placenta from mother to fetus).
– If fetal infection has been confirmed or is highly suspected,
pyrimethamine and sulfadiazine are used for treatment and
decrease in disease severity.
•
•
•
•
Do not eat undercooked meat.
Wash hands after handling raw meat.
Keep children's play areas free from cat and dog feces.
Wash your hands thoroughly after touching soil that may be
contaminated with animal feces.